Seminars & Events

Friday, October 4, 2013: Dr. Laurie Ryan, SMCM '86 (National Institute on Aging) will speak on "Alzheimer's Disease: Targets and Treatments" at 3:00 pm in Goodpaster Hall 195.

Monday, October 21, 2013: Dr. Greg Elmer (University of Maryland Baltimore) will speak on "Domains and Constructs in Motivation: Where Does the Habenula Fit In?" at 4:45 pm in Goodpaster Hall 195

Friday, October 25, 2013:  Dr. Terry Davidson (American University) will speak on "Why We Overeat and Become Obese?  It Could be What We Think!" at 3:00 pm in Goodpaster Hall 195.


Alumni Highlight

Dr. Gwen Calhoon '06 recently received her Ph.D. in Neuroscience from the University of Maryland Baltimore, and was inducted into Nu Rho Psi.







SMP Spotlight

Katie Gluskin and Jeff Haus present their SMP
Katie Gluskin and Jeff Haus, "Entorhinal Cortex Lesions, Habituation, and Latent Inhibition," 2013. Gluskin and Haus, the 2013 co-winners of the Neuroscience Award, infused a neurotoxin into the entorhinal cortex of rats to induce a lesion, and measured the resulting habituation and latent inhibition behavior within a fear conditioning paradigm.


Romano, Alison (2012).  Modeling disorders with the DIVA model : ataxic dysarthria. (Mentor: A. Jamieson)


This study examined the efficacy of the “directions into velocities of articulators” (DIVA) model, a neurologically plausible [artificial neural network] model of speech production, for studying a motor speech disorder known as “ataxic dysarthria”. Utilizing similar lesioning paradigms as used for DIVA models of stuttering and child deviations from adult speech, we set the connection weights of the critical neurological areas - the cerebellum and its cortical connections - to zero. Three lesions were made: one full cerebellar lesion, one lesion that destroyed the cerebellar neurons used to control auditory timing, and one lesion that destroyed the cerebellar neurons used to control somatosensory timing. The intact model and each of the lesioned models were taught five speech productions, which were recorded and compared based on formant analyses, pitch analysis, and voice analyses. Many of the productions were found to be differentially and significantly affected by the three lesions on many of the acoustic analyses (p<0.001 for many comparisons). Even though the lesions did not display the exact impairments as would be expected from a dysarthric speaker, it seems promising that by creating a lesion that combines elements of the auditory and somatosensory cerebellar lesions, we may be able to more accurately model ataxic dysarthria. With the proposed changes to the model, as well as the proposed future work, this line of research has many implications for modeling, understanding, and eventually treating ataxic dysarthria.